Case Report: Is It Cardiac Sarcoidosis or COVID-19 Myocarditis?

A follow-up cardiac PET scan six months later showed complete resolution of active cardiac sarcoidosis, with improvement in EF to 40–45% on echocardiogram. Prednisone was weaned.

The patient developed a COVID-19 infection a few months later that did not require hospitalization.

A surveillance cardiac PET/CT scan four months after the infection showed interval development of metabolic activity within the basal anterior wall, mid to basal anterolateral wall, basal lateral and inferolateral regions, suggesting active cardiac sarcoidosis without evidence of extracardiac sarcoidosis. An echocardiogram showed worsening EF of 30–35%, with regional wall motion abnormalities and severely hypokinetic basal segments of the anterior and anterolateral walls.

He was restarted on prednisone taper, and mycophenolate was increased from 2 g daily to 3 g daily. His follow-up PET/CT scan showed no evidence of cardiac or extracardiac

sarcoidosis, and an echocardiogram showed improved EF of 40–45%.

Discussion

Mechanisms of COVID-19 mediated myocarditis include direct viral injury, systemic inflammation causing cytokine storm, stress-induced cardiomyopathy and microvascular thrombosis that can be focal or diffuse.^1,2,5 Myocardial injury is most often seen later in the disease course, sometimes occurring several days after initial symptoms.

This image shows increased cardiac 18FDG uptake on the PET/CT nuclear scan without evidence of extracardiac inflammatory changes. (Click to enlarge.)

Even those who have clinically recovered from COVID-19 can have subclinical myocarditis. Depending on the extent of myocardial damage and time course of the disease, cardiac MRI abnormalities include diffuse myocardial edema, seen as regional or global hyperintensity; hyperemia, as evidenced by early gadolinium enhancement; and fibrosis, seen as a foci of late gadolinium enhancement.^4-6 These findings depend on the extent of myocardial damage and time course of the infection. Similar imaging findings are seen in cardiac sarcoidosis, which has a high rate of recurrence with prednisone tapering.

It remains unclear whether the myocardial uptake seen on the PET/CT scan in our case was secondary to COVID-19 myocarditis vs. cardiac sarcoidosis, or whether COVID-19 plays a role in inducing the inflammatory process of sarcoidosis, although given the similar distribution of involvement with this patient’s prior cardiac sarcoidosis flares, one of the latter two scenarios seems more likely. Data on COVID-19 in patients with cardiac sarcoidosis are scarce, and further research is required to better understand the cardiac sequalae of this infection, as well as the effects of immunosuppressive therapies in these patients (see Figures 1 and 2).³